Cancer cells under endoplasmic reticulum (ER) stress activate the UPR, which is composed of the binding immunoglobulin protein (BiP) and three major branch pathways, including the PRKR-like ER kinase (PERK), inositol-requiring enzyme 1 (IRE1), and activating transcription factor 6 (ATF6) pathways [4–7]. This evidence concerns the gene ATF6 and cancer.